Risperidone-induced type 2 diabetes presenting with diabetic ketoacidosis

A 28-year-old male presented with 2 days of vomiting and abdominal pain, preceded by 2 weeks of thirst, polyuria and polydipsia. He had recently started risperidone for obsessive-compulsive disorder. He reported a high dietary sugar intake and had a strong family history of type 2 diabetes mellitus...

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Main Authors: Clarissa Ern Hui Fang, Mohammed Faraz Rafey, Aine Cunningham, Sean F Dinneen, Francis M Finucane
Format: Article
Language:English
Published: Bioscientifica 2018-05-01
Series:Endocrinology, Diabetes & Metabolism Case Reports
Online Access:https://www.edmcasereports.com/articles/endocrinology-diabetes-and-metabolism-case-reports/10.1530/EDM-18-0031
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author Clarissa Ern Hui Fang
Mohammed Faraz Rafey
Aine Cunningham
Sean F Dinneen
Francis M Finucane
author_facet Clarissa Ern Hui Fang
Mohammed Faraz Rafey
Aine Cunningham
Sean F Dinneen
Francis M Finucane
author_sort Clarissa Ern Hui Fang
collection DOAJ
description A 28-year-old male presented with 2 days of vomiting and abdominal pain, preceded by 2 weeks of thirst, polyuria and polydipsia. He had recently started risperidone for obsessive-compulsive disorder. He reported a high dietary sugar intake and had a strong family history of type 2 diabetes mellitus (T2DM). On admission, he was tachycardic, tachypnoeic and drowsy with a Glasgow Coma Scale (GCS) of 10/15. We noted axillary acanthosis nigricans and obesity (BMI 33.2 kg/m2). Dipstick urinalysis showed ketonuria and glycosuria. Blood results were consistent with diabetic ketoacidosis (DKA), with hyperosmolar state. We initiated our DKA protocol, with intravenous insulin, fluids and potassium, and we discontinued risperidone. His obesity, family history of T2DM, acanthosis nigricans and hyperosmolar state prompted consideration of T2DM presenting with ‘ketosis-prone diabetes’ (KPD) rather than T1DM. Antibody markers of beta-cell autoimmunity were subsequently negative. Four weeks later, he had modified his diet and lost weight, and his metabolic parameters had normalised. We reduced his total daily insulin dose from 35 to 18 units and introduced metformin. We stopped insulin completely by week 7. At 6 months, his glucometer readings and glycated haemoglobin (HbA1c) level had normalised.
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spelling doaj.art-2fe9b27681b74ce497d592ec337aaae12022-12-22T02:01:09ZengBioscientificaEndocrinology, Diabetes & Metabolism Case Reports2052-05732052-05732018-05-01111410.1530/EDM-18-0031Risperidone-induced type 2 diabetes presenting with diabetic ketoacidosisClarissa Ern Hui Fang0Mohammed Faraz Rafey1Aine Cunningham2Sean F Dinneen3Francis M Finucane4Bariatric Medicine Service, Centre for Diabetes, Endocrinology and Metabolism, Galway University Hospitals, Galway, IrelandBariatric Medicine Service, Centre for Diabetes, Endocrinology and Metabolism, Galway University Hospitals, Galway, Ireland; HRB Clinical Research Facility, National University of Ireland Galway, Galway, IrelandBariatric Medicine Service, Centre for Diabetes, Endocrinology and Metabolism, Galway University Hospitals, Galway, IrelandBariatric Medicine Service, Centre for Diabetes, Endocrinology and Metabolism, Galway University Hospitals, Galway, Ireland; HRB Clinical Research Facility, National University of Ireland Galway, Galway, IrelandBariatric Medicine Service, Centre for Diabetes, Endocrinology and Metabolism, Galway University Hospitals, Galway, Ireland; HRB Clinical Research Facility, National University of Ireland Galway, Galway, IrelandA 28-year-old male presented with 2 days of vomiting and abdominal pain, preceded by 2 weeks of thirst, polyuria and polydipsia. He had recently started risperidone for obsessive-compulsive disorder. He reported a high dietary sugar intake and had a strong family history of type 2 diabetes mellitus (T2DM). On admission, he was tachycardic, tachypnoeic and drowsy with a Glasgow Coma Scale (GCS) of 10/15. We noted axillary acanthosis nigricans and obesity (BMI 33.2 kg/m2). Dipstick urinalysis showed ketonuria and glycosuria. Blood results were consistent with diabetic ketoacidosis (DKA), with hyperosmolar state. We initiated our DKA protocol, with intravenous insulin, fluids and potassium, and we discontinued risperidone. His obesity, family history of T2DM, acanthosis nigricans and hyperosmolar state prompted consideration of T2DM presenting with ‘ketosis-prone diabetes’ (KPD) rather than T1DM. Antibody markers of beta-cell autoimmunity were subsequently negative. Four weeks later, he had modified his diet and lost weight, and his metabolic parameters had normalised. We reduced his total daily insulin dose from 35 to 18 units and introduced metformin. We stopped insulin completely by week 7. At 6 months, his glucometer readings and glycated haemoglobin (HbA1c) level had normalised.https://www.edmcasereports.com/articles/endocrinology-diabetes-and-metabolism-case-reports/10.1530/EDM-18-0031
spellingShingle Clarissa Ern Hui Fang
Mohammed Faraz Rafey
Aine Cunningham
Sean F Dinneen
Francis M Finucane
Risperidone-induced type 2 diabetes presenting with diabetic ketoacidosis
Endocrinology, Diabetes & Metabolism Case Reports
title Risperidone-induced type 2 diabetes presenting with diabetic ketoacidosis
title_full Risperidone-induced type 2 diabetes presenting with diabetic ketoacidosis
title_fullStr Risperidone-induced type 2 diabetes presenting with diabetic ketoacidosis
title_full_unstemmed Risperidone-induced type 2 diabetes presenting with diabetic ketoacidosis
title_short Risperidone-induced type 2 diabetes presenting with diabetic ketoacidosis
title_sort risperidone induced type 2 diabetes presenting with diabetic ketoacidosis
url https://www.edmcasereports.com/articles/endocrinology-diabetes-and-metabolism-case-reports/10.1530/EDM-18-0031
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AT ainecunningham risperidoneinducedtype2diabetespresentingwithdiabeticketoacidosis
AT seanfdinneen risperidoneinducedtype2diabetespresentingwithdiabeticketoacidosis
AT francismfinucane risperidoneinducedtype2diabetespresentingwithdiabeticketoacidosis